Centrophenoxine - the anti-aging brain booster
  by James South MA

Centrophenoxine (meclofenoxate) is a compound of dimethylaminoethanol (DMAE) and parachlorophenoxyacetate (pCPA).  Dimethylaminoethanol is a natural food component, found especially in fish, and is also a natural metabolite of the human body.  Centrophenoxine's other half, pCPA, is a synthetic compound similar to a variety of plant hormones called "auxins."

Centrophenoxine Lipofuscin remover       

One of the earliest discoveries from animal studies showed that centrophenoxine is extremely effective at reducing lipofuscin levels. Lipofuscin is a "garbage residue" biochemical conglomerate that accumulates over a lifetime, sometimes reaching 30% of the cell volume in aged animals.

As cells accumulate ever more lipofuscin they become ever less functional, and they may die rapidly when a critical threshold of lipofuscin accumulation is reached.

Animal studies have shown centrophenoxine to be highly efficient at removing this cellular garbage- notable reductions in mice occur within 6 weeks. One study with aged rats found a 28-42% reduction in brain lipofuscin levels after 8 weeks of centrophenoxine treatment.

Both human and animal studies have shown that low lipofuscin levels correlate with healthy cellular function, while high lipofuscin accompanies poor cellular health.

Through a variety of animal experiments measuring learning abilities and memory, aged animals whose high lipofuscin levels were reduced by centrophenoxine, also had their memory and learning abilities restored to a level similar to healthy young animals, while untreated high lipofuscin control animals did not.

Centrophenoxine Cognition enhancement

The chief component of centrophenoxine is DMAE which is part of the choline betaine cycle, natural to human and animal cells.

By adding a methyl group (CH3) to DMAE, choline (also called trimethylaminoethanol) is formed. The choline thus formed may then be used to make other valuable biochemicals, such as the major neurotransmitter acetylcholine, or the essential membrane constituents phosphatidylcholine and sphingomyelin.

Choline can also be oxidized to make betaine (trimethylglcine), important for ridding the body of heart and artery toxic homocysteine, now considered one of the most important risk factors for heart disease.

Under fasting conditions, normal blood levels of choline range from 8 to 12 micromoles.  When blood choline levels are below 14 micromoles, choline flows from brain cells into the bloodstream. When blood choline levels are above 14 micromoles, choline flows from the blood into the brain.

Unfortunately, when choline enters the blood from brain cells, it is derived from auto-cannibalization, the choline containing phospholipids (which are critical brain cell membrane components) are broken down to provide the choline entering the blood.

There is evidence that excessive neuronal choline auto-cannibalization over a lifetime may contribute to Alzheimer's disease.

Centrophenoxine The need for supplementation

While a natural foods diet, such as liver, meat and eggs provides high dietary levels of choline, the modern processed junk food/ synthetic diet provides little choline, as do vegetarian diets.

Simple choline supplements, such as choline chloride or bitartrate are often broken down, as much as 60%, by gut bacteria. Thus, centrophenoxine derived DMAE is an especially ideal source of blood and brain choline for several reasons.

Gut bacteria do not digest DMAE, thus avoiding that wasteful trap. The liver quickly and easily converts DMAE to choline as needed. Also, DMAE prevents choline from being irreversibly oxidized to betaine, further raising blood choline levels. Lastly, DMAE passes through the blood brain barrier far more easily than choline.

DMAE may be incorporated into brain cell membranes, where it functions as a powerful hydroxyl free radical scavenger. Or the brain cells may convert the DMAE to choline for their needs. With the help of an enzyme called "CAT", choline is converted to the learning/ memory neurotransmitter acetylcholine.

With aging, and even more so with Alzheimer's disease, cholinergic neurons tend to under produce acetylcholine. Fortunately, the popular brain nutrient acetyl L-carnitine that powerfully increases CAT activity, thus increasing acetylcholine production.

The research of Dr. Raymond Bartus has shown that the original nootropic drug- piracetam works much more effectively to enhance learning and memory when combined with a cholinergic compound.

Thus, centrophenoxine, piracetam and acetyl-L-carnitine would be an "all star" combination for cognition enhancement.  Human studies have found centrophenoxine to be effective at restoring intellectual well being.

Centrophenoxine The human response

One study with 76 healthy elderly, who suffered from significant intellectual deterioration, found that centrophenoxine increased storage of new information into long term memory, while also increasing vigilance and alertness, after only several weeks of treatment.

A double blind placebo controlled study found clinical improvement from CPX in 7 out of 30 patients with senile psychosis.

Centrophenoxine Much more than DMAE

Centrophenoxine, which is more than just DMAE, also has a general activating effect on brain function. Centrophenoxine enhances neuronal glucose (the chief brain fuel) and oxygen uptake, while increasing carbon dioxide production, all signs of increased brain ATP production.

Centrophenoxine also increases neuronal RNA and protein production. RNA (derived from DNA in the cell nucleus) "instructs" neurons how to form proteins which help encode memory, as well as repair cell damage.

Yet brain RNA and protein production normally drop with age, and especially when large lipofuscin deposits form around the cell nucleus, one of the main sites where lipofuscin accumulates in old age.

Centrophenoxine reverses this age-related drop. It is interesting to note here that the pCPA component of CPX is similar to plant auxins- plant hormones, which increase RNA and protein production in growing plants.

Centrophenoxine has been shown to increase repair of the synapses that connect nerve cells to each other- while untreated aging synapses tend to deteriorate in number, structure and function.

Thus, because of the unique plant auxin like substance pCPA that is combined with DMAE to make centrophenoxine, centrophenoxine may be considered the ultimate "DMAE plus."

Centrophenoxine the dosages

In spite of the generally beneficent anti-aging, brain energizing, repairing effects of centrophenoxine, a few words of caution are necessary.

Centrophenoxine is a powerful enhancer of brain and peripheral nervous system acetylcholine levels, and too much acetylcholine can cause problems. Excessive acetylcholine levels can lead to headaches, neck, jaw and shoulder muscle tension, insomnia, irritability and hyper excitability, agitation and restlessness.

If any of these occur, simply discontinue centrophenoxine for a few days and then try a reduced dosage. Also, those with major depression, mania, seizure disorders or Parkinson's disease should avoid centrophenoxine, as too much acetylcholine may worsen these conditions. Also, pregnant women should avoid centrophenoxine.

While elderly people with significant intellectual decline/ loss of vigor may need 3 to 6 centrophenoxine tablets per day (250mg each), taken preferably with breakfast and lunch, in order to avoid insomnia.

For healthy younger people simply wishing the brain protection/ cognitive boost/ choline benefits that centrophenoxine provides may need only 1 or 2 centrophenoxine tablets (250mg each) daily with breakfast or lunch.

To avoid any slight acetylcholine excess that may slowly creep up unnoticed, it may be helpful to skip centrophenoxine one or two days weekly.

Effects on aging mammalian brain

J. AM. GERIATR. SOC. (USA), 1978, 26/2 (74-81)

A study was made of the effects of centrophenoxine on the learning and memory of old mice. The results were correlated with changes in neuronal lipofuscin in the cerebral cortex and hippocampus. Old female mice (11-12 months) were treated with centrophenoxine for three months and their learning and memory were tested in a T-maze. The number of trials required to attain the criterion in the 20 treated old mice were compared with those for 20 untreated mice of the same age and for 20 younger untreated mice. The treated animals learned the task with significantly fewer trials, and also exhibited a reduction of neuronal lipofuscin pigment in both the cerebral cortex and the hippocampus. The changes in lipofuscin were demonstrated by study of the characteristic autofluorescence, and by histochemical and ultrastructural (electron microscope) observations.




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